Inflammation is the foundation for cancer and degenerative/autoimmune diseases. Small changes in diet and exercise, e.g. omega-3 oils, vitamin D, low starch, and maintaining muscle mass, can dramatically alter predisposition to disease and aging, and minimize the negative impact of genetic risks. Based on my experience in biological research, I am trying to explain how the anti-inflammatory diet and lifestyle combat disease. 190 more articles at http://coolinginflammation.blogspot.com

Anti-Inflammatory Diet

All health care starts with diet. My recommendations for a healthy diet are here:

Saturday, March 14, 2009

Insulin-producing cells of the pancreases of diabetics have been found to harbor viruses common to the gut. Antibodies to the virus coat proteins also bind to pancreas proteins.

A recent paper, referenced below, shows that in a collection of samples from the pancreases of individuals that had been diagnosed with type I diabetes less than one year prior to the sampling, insulin producing cells are also infected with enterovirus. The same association between enterovirus infection was found to a lesser extent in type II diabetics, but not in non-diabetic controls.

Enteroviruses have been repeated associated with diabetes over the last decade and antigenic determinants of the enterovirus protein coat also bind, i.e. cross react, with antigenic determinants of human cellular proteins.

I examined the enterovirus coat protein, VP1, and found the same three amino acid sequence (three basic amino acids, lysine [K] or arginine [R], highlighted) that I also found in all allergens (peanut, ragweed, dust mite, bee venom) and autoantigens of autoimmune diseases (lupus, MS), and is associated with heparan sulfate-based internalization and presentation of protein immunogens. This observation is consistent with my hypothesis that inflammation plus the presence of one of these proteins, results in production of B and T lymphocytes specific for antigenic determinants on the surface of the immunogen protein. Note that the antigenic determinants usually do not include the three basic amino acid sequence, e.g. RRK, that is involved in uptake and presentation of the protein.

Thursday, March 5, 2009

It is hard to sort out the inflammatory effects of short/long-chain omega-6 and omega-3 fatty acids. Vegetable antioxidants make the picture even worse. The absolute, as well as relative amounts, of the various types of fatty acids make a difference. It also now appears that oxidation prior and during digestion may be important to the impact of polyunsaturated fatty acids (PUFAs). The source (perhaps even the meal composition) of the PUFAs was as important as omega-3 versus omega-6, for common, short chain PUFAs.

In some studies, omega-3 PUFAs, such as the short-chain alpha linolenic acid (ALA) common in flax seed or the long-chain fish oil FUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduced cancer in human and mice. Earlier work in cell cultures showed that all of PUFAs suppressed the growth of cancer cells.

A large French study (reference below) began in 1993. Approximately 100,000 women between the ages of 40 and 65 volunteered to provide dietary and breast malignancy information and ca. 75,000 qualified for the study (the French component of EPIC, European Investigation of Cancer and Nutrition) . The dietary data provided information on the fatty acid composition of meals and revealed who was eating vegetable antioxidants and vitamins.

Long chain omega-3 fatty acids (EPA and DHA) reduced breast cancer in the group of women with the highest consumption of omega-6 PUFAs.

High LA or ALA consumption in the form of vegetable oils or vegetables reduced cancer incidence.

High LA or ALA consumption in the form of processed foods or nuts was associated with a higher incidence of breast cancer.

Longer chain PUFAs were not associated with increased risk, regardless of source.

What does this mean?

The source of the PUFA is of paramount importance. This study may apply more specifically to cancers and less to other inflammation-based degenerative diseases. The general anti-inflammatory diet may need refinement. I would suggest the following additions:

Retain the preference for the more omega-3 friendly olive oil or perhaps flax oil versus the omega-6 rich vegetable oils (corn, soy, safflower), but focus on freshness and do not heat these oils.

The data seem to be in favor of saturated fats for cooking. That means a shift to coconut oil.

Vegetable antioxidants may be most important in the gut during digestion. Do these antioxidants even enter the blood stream? Certainly some alkaloids get to the brain, but much of the impact of the less mobile, large molecules may be restricted to the gut.

An extension of this discussion may be to encourage eating more leafy vegetables with meat. That may be the paleo-diet connection.

Wednesday, March 4, 2009

With the resurgence of the paleolithic diet, perhaps we should also consider paleolithic hygiene. The shaping of flint points was accomplished by skillful removal of ultrasharp (in excess of razor-sharp) flakes of glassy material. The artisan flint-knappers were community treasures, but they were banned from living near others, because they were also habitual child killers. Ingestion of flint flakes is lethal and the inherent flakiness of flint-knappers made them personae non gratae. Children living near flint-knappers died at an alarming rate and flint-knappers never sired offspring who didn’t whither and die.

Wise communities cherished flint-knappers, but they got the point and kept the knappers at a distance.

Constant Selection for New Pathogens

Where do bacterial pathogens come from and how are they spread? Some pathogenic bacteria are harbored by other animal species that humans encounter. We can pick up bacteria from pets, barnyard animals and game. We routinely place large numbers of humans in contact with every ecological niche on the planet and transport any bacteria that can grow humans rapidly to population centers. The human gut provides a mixing bowl where newly acquired bacteria are systematically extracted for their genes and recombined with resident bacterial genomes. Within days new bacteria are ready for testing in the new environment.

The most potent selection agents are antibiotics. After antibiotic treatment, only bacteria, both old residents, new arrivals, with resistance, will survive. New arrivals that incorporate the antibiotic resistance of residents will be immediately successful. New arrivals that enter with previously acquired resistance will be immediate successes and spread to fill niches vacated by antibiotic-sensitive residents.

Should Nurses and Doctors Be Quarantined?

Nurses and doctors who routinely touch patients and inhale the atomized bacterial mist around patients, receive a continuous inoculum of problematic bacteria. Healthcare practitioners are, however, immune to most of these potential pathogens by virtue of their highly educated immune systems. Unfortunately they do not get sick, but they are still potentially infectious. Their gut flora and the bacteria on their other surfaces are potential sources of the pathogens that they have acquired in their duties. Every contact with healthcare practitioners or by chronic exposure, to members of their immediate families, is potentially compromising to anyone with a compromised immune system.

The public deserves to be healthier after treatment with a healthcare professional. It is therefore mandatory that the bacteria received from a nurse or doctor through professional (or informal) contact be safe and healthy. It should be an expectation that healthcare professionals have guts that are clean-running and sanitary. To that end, it seems reasonable to routinely screen their resident bacteria and if necessary replace it with a health-promoting alternative.

We expect professional athletes to be free of performance enhancing drugs. It makes sense that doctors and nurses be free of pathogens.

Listen to my podcast on Jimmy Moore's Livin' La Vida Low Carb Show

Follow by Email

Art's Book Picks:

About Me

I grew up in San Diego and did my PhD in Molecular, Cellular and Developmental Biology (U. Colo. Boulder). I subsequently held postdoctoral research positions at the Swedish Forest Products Research Laboratories, Stockholm, U. Missouri -Colombia and Kansas State U. I was an assistant professor in the Cell and Developmental Biology Department at Harvard University, and an associate professor and Director of the Genetic Engineering Program at Cedar Crest College in Allentown, PA. I joined the faculty at the College of Idaho in 1991 and in 1997-98 I spent a six-month sabbatical at the National University of Singapore. Most recently I have focused on the role of heparin in inflammation and disease.